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Monday, June 20, 2011

Acne

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Acne
Acne is a common skin condition that afflicts most people, to a varying degree, during the teen years. However, the disease is by no means restricted to this age group; adults in their 20's or 30's may have acne. Don't think that because acne is common, treatment is unnecessary. Waiting to "outgrow" acne can be a serious mistake. Medical treatment can improve your appearance and self esteem, and prevent the development of lifelong scars.The Cause of AcneAcne is actually caused by a combination of several factors:

Rising hormone levels during adolescence cause enlargement and over activity of the oil glands in the skin.
The canals that bring this oil to the surface become blocked with keratin (a protein that is part of the skin).
When these oil glands are overactive and the canals are blocked, the bacteria that normally live on the skin and in the oil become trapped. They subsequently multiply, and cause inflammation and irritation.Cleansing and CosmeticsEven though you may be told to wash frequently, acne is not a disease caused by dirt. For example, the blackness of a blackhead is not dirt, but is due to the accumulation of the normal skin pigment in the oil gland ducts.Wash your face with a mild antibacterial soap recommended by your dermatologist twice a day. If one's skin is very oily, it may be washed more often. Over washing or scrubbing tends to irritate the skin and will make acne worse. Therefore, do not use any abrasive cleaners or cleansing pads.Shampooing is also important in acne therapy. The oilier your hair is, the more often you should shampoo it. Also, it is best to keep hair off the face as much as possible to avoid hair oils.For covering blemishes, many preparations have been formulated to match skin color. These cosmetics should be water based (i.e. the first ingredient on the label should be water). Most cosmetics and skin products that are safe to use on acne-prone skin will say “non-comedogenic”, “oil free” or “won’t clog pores.”Look for these labels on your facial products. Greasy applications such as Vaseline, cocoa butter, cold cream, and vitamin E oil should be avoided. If the face is dry, your dermatologist can recommend a moisturizer for your type skin.

Diet : The idea that acne can be brought on by an unhealthy diet has been debated for years. For the last 30 years the conventional wisdom has been that diet plays no role in most cases of acne. While many Dermatologists still believe this to be true, another view is emerging. Doctors were surprised to learn that acne is virtually unknown in some remote jungle tribes. These people live off the land without the modern staples of beef, dairy, wheat and sugar. On the other hand, the age when acne first emerges is getting younger for teens in the USA along with the age of puberty.Could something in the modern diet be the culprit? Some say yes, because eating the wrong things can let loose the wrong kind of hormones.These hormones activate the oil glands in your face. High levels of hormones are present in cows milk, since most dairy cattle are pregnant. The idea that milk is an essential part of everyone's diet is probably wrong. You can easily get your calcium, vitamin D and protein from other foods, or from supplements. It may take 6 months off all dairy products before any improvement can be seen, but about 1 in 3 say this helps their acne quite a bit.

Another theory blames sugar and excess carbohydrates. These push your body to pump out insulin, which can throw off other hormones as a result. Someoverweight women with acne have hormone imbalances and excess insulin. In these women bringing the insulin level down corrects the hormone levels and acne. While there is no proof sugar and carbohydrates are important in most cases of acne, there is also no doubt sugar and excessive carbohydrates are not good for you. Eating healthy foods is a good ideafor acne sufferers.There are still others who blame particular foods for their acne. Chocolate and nuts are commonly mentioned, but these don't seem to play arole in most people's acne. The importance of diet may vary between individuals, but the idea that diet plays no role in acne is probably on the way out.

Treatment of Acne :
Acne need not be feared as something untreatable. In recent years many effective forms of therapy have been developed. Dermatologists want to prevent scars that acne can leave. Years of untreated acne can leave a lifelong imprint on a person's face and can have an effect on his or her self-image. While acne may not be curable, it is usually controllable.Since acne has many forms, your dermatologist designs an individual approach to care for successful control. Thus, the course of therapy will vary according to such factors as type of acne, it's severity and extent, and the patient's day-to-day activities.

Mild acne is treated with one or a combination of topical medications. The purpose of these is not only to treat existing acne lesions, but to prevent new blemishes from forming. Therefore, these are applied over most of your face, not just directly on the present pimples. In addition, in some people these creams may cause the face to become a little dry, pink or feel taught. This is normal. If your face becomes too irritated or 'raw' feeling, don't stop the creams, just decrease the frequency of application (i.e. apply every second or third day).Moderate and severe acne is usually treated by topical medicines with the addition of oral antibiotics. Since different combinations work better for some patients than others, you are usually evaluated every four to six weeks until the acne is well controlled.In addition to this conventional therapy, your dermatologist may recommend one or more of these treatments to speed healing and clearing of your acne:

Acne Surgery: This procedure greatly speeds acne clearing and appearance by manually removing blackheads and whiteheads. A round loop extractor is used to apply uniform smooth pressure to dislodge the material. Inserting a pointed instrument to carefully expose the contents loosens lesions that offer resistance. This may be combined with microdermabrasion, which helps to remove dead skin on the face and open up smaller blocked pores.

Intralesional Corticosteroid Therapy: If one or several painful acne cysts develop, fast relief is available with this relatively painless procedure. Each cyst is given a single injection of a dilute cortisone solution, using a very tiny needle.

Accutane Therapy: In 1982 a new oral medication, isotretinoin (Accutane), became available for the treatment of patients with severe acne not responsive to conventional treatments. The duration of treatment is usually five to six months, and one such course is often curative of severe acne forever. Use of this medication does require a thorough understanding of its side effects and precautions (e.g. the prevention of pregnancy).Treatment of Acne ScarringPrior to correcting acne scarring, it is generally advisable to wait until acne activity has been low or absent for several months. Scars improve with time as the body softens their appearance. The color contrast is often the most troublesome aspect of resolving large acne blemishes. These lesions may leave a flat or depressed red scar that is so obvious, patients mistake the mark for an active lesion. The color will fade and approach skin tones in 4 to 12 months. Many patients are self-conscious about the pitted and crater like scars that do not fade. These remain as a permanent record of previous severe acne. Your dermatologist may a variety of procedures to you to remove or revise these marks:

Chemical Peel: Superficial acne scarring, and irregular pigmentation of the skin are easily treated with this technique. Chemical agents are applied to the skin, which cause the outer layer to be removed. Different chemicals and concentrations are used, depending on ones skin type and degree of scarring.

Laser Resurfacing: More prominent scarring from acne is best treated by this technique. The top several layers of skin are removed with this high energy light. This action evens out the skin to give it a smoother, more pleasing contour.

Punch Excision and/or Grafting: Some narrow pitted scars are too deep to be removed by dermabrasion. These can be removed with a surgical instrument called a punch. The resulting defect is closed, either primarily or with a tiny skin graft, with gratifying results. Sometimes this procedure is followed by chemical peel or laser resurfacing for patients with a mixed type of scarring.

Collagen Implantation: Patients with a few soft depressed scars with smooth edges respond well to collagen. This natural protein is injected under the lesion to elevate it to the level of the skin.A Final WordTreatment of acne is a continuing process if the disorder is to be controlled successfully. You must follow your dermatologist's instructions, since you are the only one who can accomplish the necessary daily care. If you are willing to spend the time and extend the effort, you can expect a pleasing result.
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Excessive Sweating

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Excessive Sweating :
Known medically as Hyperhidrosis :About 1% and some say 2% of people all over the world complain of excessive sweating , and because this is a high percentage , we will talk about this problem , its presentation , causes and treatment.


Presentation : The typical presentation is an excessive sweating that commonly affects : hands "palmer" , feet "planter" and armpits "axillary" and less commonly face , forehead and other areas. It could occur without any identified reason (such as heat , hyperactivity , anxiety or emotional stress).
Sweating usually subsides during sleeping and comes back again after waking up .

Sweating is embarrassing, it stains clothes, and it complicates business and social interactions. Severe cases can have serious practical consequences as well, making it hard for people who suffer from it to hold a pen, grip a steering wheel, or shake hands.

Causes :
Many diseases can cause excessive sweating , such as hyperthyroidism , but patients in this case have other complaints for example : heat intolerance , weight loss , diarrhea ... etc.
TB and Malignancies cause night sweating not day sweating. Emotional stress can trigger sweating but it subsides once the cause of the stress goes.


In general most cases of occur in people who are otherwise healthy , and it tends to affect more than one member of the same family which means that hereditary factors have a role.


Mechanism :As we know we have in our bodies the autonomous nervous system. This system on which we have no control affects blood pressure, heart rate, anxiety level and many other functions.. it's divided into 2 parts : the sympathatic "that trigger sweating" and the parasympathetic.
In hyperhidrosis patient has over activation of the Sypmathatic nervous system.


Treatment :1) Local treatment with Aluminium chloride containing antiperspirants such as ANHYDROL solution : it's very effective mainly in the axillary area . You have to use it for 4 times in the first week "once per day" to notice the results , then use it 2 times in the second week and 1 time for every week later.
Aluminium chloride causes sever skin irritation so to avoid this side effect you have to ensure that your armpits are totally dry before using it, then apply a very thin layer of the agent over the targeted area "armpit" and keep your arms raised or put your hands behind your head and lie on the bed until it dries completely "it takes 5 - 10 minutes" .
It's advised to use it just before going to bed because the parasympathetic system takes the lead over the sympathetic system during sleeping and there will be no sweating and no skin irritation , then washing it after waking up by taking a hot bath.

2) Injections of botulinum toxin type A, under the brand names Botox or Dysport, are used to disable the sweat glands.The effects may persist from four to nine months depending on the site of injection. This procedure has been approved by the U.S. Food and Drug Administration (FDA) to treat underarm sweating. It's also most effective in the axillary area.


3) Surgical procedures
Sweat gland removal or destruction is one surgical option available for axillary hyperhidrosis. There are multiple methods for sweat gland removal or destruction such as sweat gland suction, retrodermal currettage, and axillary liposuction, Vaser, or Laser Sweat Ablation. Sweat gland suction is a technique adapted from liposuction, in which approximately 30% of the sweat glands are removed, with a proportionate reduction in sweat.

There are other choices of treatment but less effective.
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Hair Loss

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Hair Loss
Introduction : The normal cycle of hair growth lasts for 2 to 3 years. Each hair grows approximately 1 centimeter per month during this phase. About 90 percent of the hair on your scalp is growing at any one time. About 10 percent of the hair on your scalp, at any one time, is in a resting phase. After 3 to 4 months, the resting hair falls out and new hair starts to grow in its place.

It is normal to shed some hair each day as part of this cycle. However, some people may experience excessive (more than normal) hair loss. Hair loss of this type can affect men, women and children.

What causes excessive hair loss?
A number of things can cause excessive hair loss. For example, about 3 or 4 months after an illness or a major surgery, you may suddenly lose a large amount of hair. This hair loss is related to the stress of the illness and is temporary. 

Hormonal problems may cause hair loss. If your thyroid gland is overactive or underactive, your hair may fall out. This hair loss usually can be helped by treatment thyroid disease. Hair loss may occur if male or female hormones, known as androgens and estrogens, are out of balance. Correcting the hormone imbalance may stop your hair loss.

Many women notice hair loss about 3 months after they've had a baby. This loss is also related to hormones. During pregnancy, high levels of certain hormones cause the body to keep hair that would normally fall out. When the hormones return to pre-pregnancy levels, that hair falls out and the normal cycle of growth and loss starts again. 

Some medicines can cause hair loss. This type of hair loss improves when you stop taking the medicine. Medicines that can cause hair loss include blood thinners (also called anticoagulants), medicines used for gout, high blood pressure or heart problems, vitamin A (if too much is taken), birth control pills and antidepressants.

Certain infections can cause hair loss. Fungal infections of the scalp can cause hair loss in children. The infection is easily treated with antifungal medicines.

Finally, hair loss may occur as part of an underlying disease, such as lupus or diabetes. Since hair loss may be an early sign of a disease, it is important to find the cause so that it can be treated.

Can certain hairstyles or treatments cause hair loss?
Yes. If you wear pigtails or cornrows or use tight hair rollers, the pull on your hair can cause a type of hair loss called traction alopecia (say: “al-oh-pee-sha”). If the pulling is stopped before scarring of the scalp develops, your hair will grow back normally. However, scarring can cause permanent hair loss. Hot oil hair treatments or chemicals used in permanents (also called "perms") may cause inflammation (swelling) of the hair follicle, which can result in scarring and hair loss.

What is common baldness?

"Common baldness" usually means male-pattern baldness, or permanent-pattern baldness. It is also called androgenetic alopecia. Male-pattern baldness is the most common cause of hair loss in men. Men who have this type of hair loss usually have inherited the trait. Men who start losing their hair at an early age tend to develop more extensive baldness. In male-pattern baldness, hair loss typically results in a receding hair line and baldness on the top of the head.

Women may develop female-pattern baldness. In this form of hair loss, the hair can become thin over the entire scalp.

Can my doctor do something to stop hair loss?

Perhaps. Your doctor will probably ask you some questions about your diet, any medicines you're taking, whether you've had a recent illness and how you take care of your hair. If you're a woman, your doctor may ask questions about your menstrual cycle, pregnancies and menopause. Your doctor may want to do a physical exam to look for other causes of hair loss. Finally, blood tests or a biopsy (taking a small sample of cells to examine under a microscope) of your scalp may be needed.

Is there any treatment for hair loss?
Depending on your type of hair loss, treatments are available. If a medicine is causing your hair loss, your doctor may be able to prescribe a different medicine. Recognizing and treating an infection may help stop the hair loss. Correcting a hormone imbalance may prevent further hair loss.

Medicines may also help slow or prevent the development of common baldness. One medicine, minoxidil (brand name: Rogaine), is available without a prescription. It is applied to the scalp. Both men and women can use it. Another medicine, finasteride, is available with a prescription. It comes in pills and is only for men. It may take up to 6 months before you can tell if one of these medicines is working.

If adequate treatment is not available for your type of hair loss, you may consider trying different hairstyles or wigs, hairpieces, hair weaves or artificial hair replacement.
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Treatment of community-acquired pneumonia in adults in the outpatient setting

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INTRODUCTION — Community-acquired pneumonia (CAP) is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community, as distinguished from hospital-acquired (nosocomial) pneumonia. A third category of pneumonia, designated "healthcare-associated pneumonia," is acquired in other healthcare facilities such as nursing homes, dialysis centers, and outpatient clinics.

CAP is a common and potentially serious illness. It is associated with considerable morbidity and mortality, particularly in elderly patients and those with significant comorbidities 

The treatment of CAP in adults in the outpatient setting will be reviewed here. A variety of other important issues related to CAP are discussed separately. These include:

 • The diagnostic approach to patients with CAP.

 • How one makes the decision to admit patients with CAP to the hospital. 

 • Treatment recommendations for CAP in patients requiring hospitalization. 

 • Treatment recommendations for patients with healthcare-associated pneumonia. 

 • The evidence for efficacy of different antibiotic medications in the empiric treatment of CAP and issues related to drug resistance. 

 • The epidemiology and microbiology of CAP. 

 • Pneumonia in special populations, such as aspiration pneumonia and immunocompromised patients. 

INDICATIONS FOR HOSPITALIZATION — Determination of whether a patient with CAP can be safely treated as an outpatient or requires hospitalization is essential before selecting an antibiotic regimen. Severity of illness is the most critical factor in making this determination, but other factors should also be taken into account. These include ability to maintain oral intake, likelihood of compliance, history of substance abuse, cognitive impairment, living situation, and patient functional status. These issues with appropriate references are discussed in detail elsewhere. 

Summarized briefly, prediction rules have been developed to assist in the decision of site of care for CAP. The two most commonly used prediction rules are the Pneumonia Severity Index (PSI) and CURB-65. The PSI is better studied and validated, but requires a more complicated assessment.

CURB-65 uses five prognostic variables:

 • Confusion (based upon a specific mental test or disorientation to person, place, or time)

 • Urea (blood urea nitrogen in the United States) >7 mmol/L (20 mg/dL)

 • Respiratory rate >30 breaths/minute

 • Blood pressure [BP] (systolic <90 mmHg or diastolic <60 mmHg)

 • Age >65 years

The authors of the original CURB-65 report suggested that patients with a CURB-65 score of 0 to 1, who comprised 45 percent of the original cohort and 61 percent of the later cohort, were at low risk and could probably be treated as outpatients; those with a score of 2 should be admitted to the hospital, and those with a score of 3 or more should be assessed for ICU care, particularly if the score was 4 or 5.

A simplified version (CRB-65), which does not require testing for blood urea nitrogen, may be appropriate for decision-making in primary care practitioners' offices. With either version, admission to the hospital is recommended if one or more points are present.

Clinical judgment should be used for all patients, incorporating the prediction rule scores as a component of the decision for hospitalization or intensive care unit admission, but not as an absolute determinant .

PRINCIPLES OF ANTIMICROBIAL THERAPY — CAP can be caused by a variety of pathogens, with bacteria being the most common identifiable cause . The choice of initial therapy is complicated by the emergence of antibiotic resistance among Streptococcus pneumoniae, the most common bacterium responsible for CAP. 
Empiric therapy — Antibiotic therapy is typically begun on an empiric basis, since the causative organism is not identified in an appreciable proportion of cases of CAP treated in the outpatient setting . In addition, the clinical features and chest radiographic findings are not sufficiently specific to determine etiology and influence treatment decisions. The sputum Gram stain can be useful for directing the choice of initial therapy if performed on a good quality sample and interpreted by skilled examiners using appropriate criteria .

The 2007 Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) guidelines on the management of community-acquired pneumonia suggest that routine tests to identify an etiology for CAP are optional for patients who do not require hospitalization . This recommendation is based in part upon the low rate of failure of empiric therapy in patients with CAP treated in the outpatient setting. The efficacy of empiric therapy was illustrated in a study of over 700 ambulatory patients treated for CAP in one of six emergency departments seen from November 2000 through April 2001, in which empiric antibiotics (a macrolide or fluoroquinolone in >88 percent) were almost universally effective, with only 2.2 percent requiring hospitalization within three weeks of initial emergency department visit .

In contrast, testing for a microbial diagnosis is important in clinical or epidemiologic settings suggesting possible infection with an organism that requires treatment different from standard empiric regimens. These include Legionella species, Mycobacterium tuberculosis, influenza A and B or avian influenza, community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA), or agents of bioterrorism .

The selection of antimicrobial regimens for empiric therapy is based upon a number of factors, including:

 • The most likely pathogen(s). 

 • Clinical trials proving efficacy.

 • Risk factors for antimicrobial resistance. The choice of empiric therapy must take into account the emergence of antibiotic resistance among Streptococcus pneumoniae, one of the most common bacteria responsible for CAP. 

 • Medical comorbidities that may influence the likelihood of a specific pathogen and may be a risk factor for treatment failure.

Additional factors that may affect the choice of antimicrobial regimen include the potential for inducing antimicrobial resistance, pharmacokinetic and pharmacodynamic properties, safety profile, and cost .

Common pathogens — Although a variety of bacterial pathogens can cause CAP, a limited number are responsible for the majority of cases

With respect to patients treated in the outpatient setting, the most frequently isolated pathogens are Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae, and respiratory viruses (eg, influenza, parainfluenza, respiratory syncytial virus) . Legionella pneumoniae and Haemophilus influenzae are less common. The "atypical" pathogens are not often identified in clinical practice because there are not specific, rapid, or standardized tests for their detection, with the exception of L. pneumophila.

Patients with CAP due to Staphylococcus aureus, Enterobacteriaceae, and Pseudomonas aeruginosa are typically sicker and require admission to the hospital. 

Risk factors for drug resistance — Risk factors for and other issues related to drug resistance in patients with CAP are discussed in detail elsewhere. 

Summarized briefly, risk factors for drug-resistant S. pneumoniae in adults include:
 • Age >65 years

 • Beta-lactam, macrolide, or fluoroquinolone therapy within the past three to six months

 • Alcoholism

 • Medical comorbidities

 • Immunosuppressive illness or therapy

 • Exposure to a child in a day care center

Recent therapy or a repeated course of therapy with beta-lactams, macrolides, or fluoroquinolones is a risk factor for pneumococcal resistance to the same class of antibiotic.

The impact of discordant drug therapy, which refers to treatment of an infection with an antimicrobial agent to which the causative organism has demonstrated in vitro resistance, appears to vary with antibiotic class and possibly with specific agents within a class. Most studies have been performed in patients with S. pneumoniae infection and suggest that current levels of beta-lactam resistance generally do not cause treatment failure when appropriate agents (eg, amoxicillin, ceftriaxone, cefotaxime) and doses are used. Of the beta-lactams, cefuroxime is a possible exception. In addition, there appears to be an increased risk of macrolide failure in patients with macrolide-resistant S. pneumoniae. 

GUIDELINES — A number of medical societies have issued guidelines for the treatment of CAP . The antibiotic regimens advocated by a collaboration between the Infectious Disease Society of America and the American Thoracic Society (IDSA/ATS) in 2007 , and guidelines from the British Thoracic Society (BTS) in 2009 are summarized here .

The following discussion will review antibiotic therapy in ambulatory patients with CAP. Guideline recommendations for therapy of patients with CAP treated in the inpatient setting are presented separately.

 • The regimens chosen by the IDSA/ATS guidelines mainly rely on macrolides (with or without a beta-lactam) or newer fluoroquinolones for outpatient therapy . The guidelines promote the use of macrolides to provide coverage for both S. pneumoniae and atypical pathogens (particularly, M. pneumoniae and C. pneumoniae), which account for the majority of cases of CAP in ambulatory patients . In studies from different regions of the world, atypical pathogens account for 20 to 30 percent of cases of CAP .

 • The BTS guidelines tend to select older antibiotics than those recommended in North America .

North American approach — The macrolides, which are effective against the atypical pathogens, are recommended in the absence of significant risk factors for macrolide-resistant S. pneumoniae. Experience in North America, suggests that macrolide-resistant S. pneumoniae is less significant for patients without comorbidities or risk factors compared to patients with risk factors . Recent use of macrolide antibiotics is considered a risk factor for resistant S pneumoniae; thus, monotherapy with a macrolide is not recommended for persons who received a macrolide antibiotic in the preceding three months. coccus pneumoniae to the macrolides, azalides, lincosamines, and ketolides".)

BTS approach — In the 2009 British Thoracic Society guidelines, the preferred drug for outpatient management is amoxicillin (500 mg orally three times daily), with doxycycline or clarithromycin as alternatives, including for those with penicillin allergy .

The rationale is that amoxicillin at these doses is effective against most strains of S. pneumoniae with decreased susceptibility to penicillin. Most of the macrolide-resistant S. pneumoniae in Europe is erm-mediated high-level resistance. As a result, the macrolides are not optimal first-line empiric agents.

Coverage of atypical pathogens — The BTS approach places less significance than the North American approach on the need to treat the atypical pathogens empirically in ambulatory patients. Initial empiric therapy that covers M. pneumoniae is considered unnecessary, since the pathogen exhibits epidemic periodicity every four to five years and largely affects younger persons.

Although the clinical course of M. pneumoniae or C. pneumoniae infection is often self-limited, these pathogens can cause severe CAP. As a result, it has been argued that appropriate treatment for even mild CAP due to Mycoplasma reduces both morbidity and the duration of symptoms.

The efficacy of empiric coverage of atypical pathogens was evaluated in a 2005 meta-analysis that evaluated 18 randomized trials of over 6700 patients with mild to moderate CAP who were assigned to treatment with either a beta-lactam or an antibiotic active against atypical pathogens . There was no overall advantage to covering atypical pathogens in terms of the rate of failure to achieve clinical cure or improvement (relative risk 0.97, 95% CI 0.87-1.07) but, in a subgroup analysis, there was a significantly lower failure rate for Legionella infection with such a regimen (relative risk 0.40, 95% CI 0.19-0.85). These trials were not designed to compare the time to response with the different regimens.

TREATMENT REGIMENS — Treatment regimens for outpatients with CAP are based upon studies of the effectiveness of antibiotics, the severity of illness, the presence of comorbid conditions, and the prevalence of risk factors for drug resistant S. pneumoniae (DRSP). 

We suggest the following approach to empiric antimicrobial therapy. 

No comorbidities or recent antibiotic use — For uncomplicated pneumonia in patients who do not require hospitalization, have no significant comorbidities and/or use of antibiotics within the last three months, and where there is not a high prevalence of macrolide-resistant strains, we recommend any one of the following oral regimens:

 • Azithromycin (500 mg on day one followed by four days of 250 mg a day); 500 mg a day for three days, or 2 g single dose (microsphere formulation) are acceptable alternative regimens

 • Clarithromycin XL (two 500 mg tablets once daily) for five days or until afebrile for 48 to 72 hours

 • Doxycycline (100 mg twice a day) for seven to 10 days

There is concern that widespread use of fluoroquinolones in outpatients will promote the development of fluoroquinolone-resistance among respiratory pathogens (as well as other colonizing pathogens) and may lead to an increased incidence of C. difficile colitis . In addition, empiric use of fluoroquinolones should not be used for patients at risk for Mycobacterium tuberculosis without an appropriate assessment for tuberculosis infection. The administration of a fluoroquinolone in patients with tuberculosis has been associated with a delay in diagnosis, increase in resistance, and poor outcomes. 

Because of these concerns, the use of fluoroquinolones is discouraged in ambulatory patients with CAP without comorbid conditions or recent antimicrobial use, unless it is known that there is a high prevalence of high-level macrolide-resistant S. pneumoniae in the local community. When such resistance is present, the regimen for patients with comorbidities or recent antibiotic use described in the next section can be followed.

Despite these recommendations, fluoroquinolones continue to be given, often inappropriately, for CAP. In one report of 768 ambulatory patients with CAP seen in an emergency department in 2000 and 2001, 245 (32 percent) were treated with levofloxacin; one-half of these patients did not meet the criteria for appropriate fluoroquinolone therapy .

Telithromycin is NOT recommended as a first-line empiric regimen because of concerns about toxicity. 

Although erythromycin is the least expensive macrolide, we rarely use this drug for three reasons: multiple daily doses over several days are required; compliance is limited by gastrointestinal side effects, as well as dosing; and there is a risk of sudden cardiac death due to QT interval prolongation, particularly when other drugs metabolized by CYP3A4 are taken concurrently . The drugs noted above are as effective, more convenient to use, and less toxic.

Comorbidities or recent antibiotic use — The presence of significant comorbidities (ie, chronic obstructive pulmonary disease [COPD], liver or renal disease, cancer, diabetes, chronic heart disease, alcoholism, asplenia, or immunosuppression), and/or use of antibiotics within the prior three months, increases the risk of infection with more resistant pathogens. We recommend one of the following oral regimens for such patients:

 • A respiratory fluoroquinolone (gemifloxacin 320 mg daily, levofloxacin 750 mg daily, or moxifloxacin 400 mg daily) for a minimum of five days.

 • Combination therapy with a beta-lactam effective against S. pneumoniae (high-dose amoxicillin, 1 g three times daily or amoxicillin-clavulanate 2 g twice daily or cefpodoxime 200 mg twice daily or cefuroxime 500 mg twice daily) PLUS either a macrolide (azithromycin 500 mg on day one followed by four days of 250 mg a day or clarithromycin 250 mg twice daily or clarithromycin XL 1000 mg once daily) or doxycycline (100 mg twice daily). Treatment should be continued for a minimum of five days. 

These regimens are also appropriate where there is a high prevalence of "high-level" macrolide-resistant S. pneumoniae, even in the absence of comorbidity or recent antimicrobial use. When choosing between fluoroquinolones, in vitro studies of moxifloxacin and gemifloxacin show more activity against penicillin-resistant pneumococci strains than levofloxacin; the clinical significance of these findings is not yet clear .

Gemifloxacin causes a rash in 2.8 percent of patients overall, but a higher rate (14 percent) in women under 40 years of age who received the drug for seven or more days. The rash is generally mild, occurs after the fifth day of therapy, and resolves with discontinuation of the agent. The rash is not associated with phototoxicity or hypersensitivity and does not preclude the use of other fluoroquinolones in the future, although repeated courses of gemifloxacin should be avoided in such patients. 

Telithromycin should be reserved as an option for patients at risk for drug-resistant pneumococcal infection in whom alternative agents are not appropriate. However, it should NOT be prescribed in patients with known liver disease. 

Pathogen-directed therapy — Once the etiology of CAP has been identified using reliable microbiologic methods, antimicrobial therapy should be directed at that pathogen .

Treatment duration and response — With respect to treatment duration, we generally agree with the 2007 IDSA/ATS guidelines. Ambulatory patients with CAP should be treated for a minimum of five days; because of the prolonged half-life of azithromycin, a shorter duration of drug administration may be indicated for this agent.

Support for this recommendation comes from a meta-analysis of 15 randomized controlled trials of almost 2800 patients with mild to moderate CAP, which found comparable clinical outcomes with less than seven days compared to more than seven days of antimicrobial therapy . Antibiotic therapy should not be stopped until the patient is afebrile for 48 to 72 hours and is clinically stable. 

Most patients with CAP begin to improve soon after the initiation of appropriate antibiotic therapy as evidenced by resolution of symptoms, physical findings, and laboratory signs of active infection . However, some symptoms often persist as the patient convalesces . This was illustrated in a study of sequential interviews in 134 ambulatory patients with CAP . The median time to resolution ranged from three days for fever to 14 days for both cough and fatigue. At least one symptom (eg, cough, fatigue, dyspnea) was still present at 28 days in one-third of patients. In another report, 76 percent had at least one symptom at 30 days, most commonly fatigue, compared to 45 percent by history in the one month prior to the onset of CAP .

These symptoms are usually not sufficient to interfere with work as illustrated in a review of 399 ambulatory patients with CAP in which the median time of return to work was six days even though one-third had at least one persistent symptom at 14 days. 

Persistence of such symptoms is not an indication to extend the course of antibiotic therapy as long as the patient has demonstrated some clinical response to treatment .

Follow-up chest radiograph — Chest x-ray findings usually clear more slowly than clinical manifestations  Routine chest x-rays for follow-up of CAP patients who are responding clinically are unnecessary. Some authorities recommend a follow-up chest x-ray at 7 to 12 weeks after treatment for selected patients who are over age 40 years or are smokers, to document resolution of the pneumonia and exclude underlying diseases, such as malignancy .

Among patients with CAP, nonresponse is primarily seen in those who require hospitalization, occurring in 6 to 15 percent of such patients. The incidence of treatment failure is not well defined in ambulatory patients with CAP because population-based studies would be required.

VACCINATION — Patients with CAP should be appropriately vaccinated for influenza and pneumococcal infection. Screening for influenza vaccination status is warranted during influenza season (eg, from October through March in the northern hemisphere) in all patients. Screening for pneumococcal vaccination status is warranted in patients age 65 or older or with other indications for vaccination. Vaccination can be performed during outpatient treatment. 

SMOKING CESSATION — Smoking cessation should be a goal for patients with CAP who smoke.


SUMMARY AND RECOMMENDATIONS

 • Most initial treatment regimens for community-acquired pneumonia (CAP) are empiric. A limited number of pathogens are responsible for the majority of cases of CAP .

 • Emerging drug-resistant S. pneumoniae (DRSP) complicates the use of empiric treatment. Treatment failures have been demonstrated with use of macrolides for macrolide-resistant organisms. We recommend not prescribing macrolide monotherapy for patients who have received a macrolide antibiotic within the preceding three months.

 • Despite in vitro resistance, penicillin-resistant pneumococci may respond to higher dose beta-lactams, other than cefuroxime. Drug toxicity limits the use of telithromycin which should be reserved for patients with "high-level" macrolide-resistant CAP in whom other agents are contraindicated. 

 • North American and British guidelines differ in their recommendations for first-line therapy for outpatient pneumonia. British guidelines promote amoxicillin and place less significance on atypical pathogens. North American guidelines advocate treating both atypical pathogens and pneumococcus, and suggest macrolides when antibiotic resistance is not anticipated. 

 • We support the IDSA/ATS guideline recommendations for empiric treatment of CAP in non-hospitalized patients:

     - For uncomplicated pneumonia in patients who have no significant comorbidities and/or use of antibiotics within the last three months, we suggest treatment with an advanced macrolide . Regimens include azithromycin (500 mg on day one followed by four days of 250 mg a day, or 500 mg for three days, or 2 g as single dose microsphere regimen) or clarithromycin XL (two 500 mg tablets once daily). We suggest NOT using fluoroquinolones for uncomplicated ambulatory patients with CAP . Alternative regimens are acceptable. 

     - For non-hospitalized patients with comorbidities or recent antibiotic use, we suggest treatment with a fluoroquinolone as monotherapy, or combination therapy with a beta-lactam plus a macrolide .

 • We recommend antibiotic treatment for a minimum of five days, although a shorter duration may be indicated with azithromycin because of its prolonged half-life. Therapy should not be stopped until the patient is afebrile for 48 to 72 hours and is clinically stable. When this is achieved, the persistence of other symptoms (eg, dyspnea, cough) is not an indication to extend the course of antibiotic therapy.
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Saturday, June 18, 2011

Acute appendicitis in adults: Clinical manifestations and diagnosis

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INTRODUCTION — Since Reginald Fitz presented the first comprehensive description of appendicitis and advocated early surgical removal of the appendix in 1886, appendicitis has been recognized as one of the most common causes of the acute abdomen worldwide. Acute appendicitis is one of the most frequent indications for abdominal surgery.

Appendicitis occurs most frequently in the second and third decades of life. The incidence is highest in the 10- to 19-year-old age group, in which it is about 233/100,000 population. It is also higher among men (male to female ratio of 1.4:1) who have a lifetime incidence of 8.6 percent compared to 6.7 percent for women .

The goal of therapy is early diagnosis and prompt operative intervention. However, the diagnosis of appendicitis can be difficult, especially in patients less than 3 years of age, pregnant, and older than age 60 years . In the younger and older age groups the diagnosis is often delayed, leading to perforation rates as high as 80 percent . The diagnosis can be challenging in pregnant women, especially in the second and third trimesters, due to the displacement of the appendix by the uterus and the resulting changes in the physical examination.

The clinical manifestations and diagnosis of appendicitis in adults will be reviewed here. The management of appendicitis, appendicitis in pregnancy, and the diagnosis and differential diagnosis of abdominal pain in adults are discussed separately.

ANATOMY — The veriform appendix is located near the ileocecal valve where the taenia coli converge on the cecum . The appendix is considered a true diverticulum of the cecum. In contrast to acquired diverticular disease, which consists of a protuberance of a subset of the enteric wall layers, the appendiceal wall contains all of the layers of the colonic wall: mucosa, submucosa, muscularis (longitudinal and circular), and the serosal covering .

The appendiceal orifice opens into the cecum. The appendix is located at the base of the cecum at the confluence of the three taenia coli. Its blood supply, the appendiceal artery, is a terminal branch of the ileocolic artery, which traverses the length of the mesoappendix and terminates at the tip of the organ .

The attachment of the appendix to the base of the cecum is constant. However the tip may migrate to the retrocecal, subcecal, preileal, postileal and pelvic positions. These normal anatomic variations can complicate the diagnosis as the site of pain and findings on the clinical examination will reflect the anatomic position of the appendix.

The presence of B and T lymphoid cells in the mucosa and submucosa of the lamina propria make the appendix histologically distinct from the nearby cecum . These cells create a lymphoid pulp that aid immunologic function by increasing lymphoid products such as IgA and operating as part of the gut-associated lymphoid tissue system . Lymphoid hyperplasia can cause obstruction of the appendix and lead to appendicitis. The lymphoid tissue undergoes atrophy with age, which may account for the age distribution seen in acute appendicitis .

PATHOGENESIS — The natural history of appendicitis is similar to that of other inflammatory processes involving hollow visceral organs. Initial inflammation of the appendiceal wall is followed by localized ischemia, perforation, and the development of a contained abscess or generalized peritonitis.

Appendiceal obstruction has been proposed as the primary cause of appendicitis . Obstruction is frequently implicated but not always required for the development of appendicitis. A study of patients with appendicitis showed that there was elevated intraluminal pressure in only one third of the patients with nonperforated appendicitis .

Appendiceal obstruction may be caused by fecaliths (hard fecal masses), calculi, lymphoid hyperplasia, infectious processes, and benign or malignant tumors. However, some patients with a fecalith have a histologically normal appendix and the majority of patients with appendicitis do not have a fecalith .

When obstruction of the appendix is the cause of appendicitis, the obstruction leads to an increase in luminal and intramural pressure, resulting in thrombosis and occlusion of the small vessels in the appendiceal wall, and stasis of lymphatic flow. As the appendix becomes engorged, the visceral afferent nerve fibers entering the spinal cord at T8-T10 are stimulated, leading to vague central or periumbilical abdominal pain . Well-localized pain occurs later in the course when inflammation involves the adjacent parietal peritoneum.

The mechanism of luminal obstruction varies depending upon the patient's age. In the young, lymphoid follicular hyperplasia due to infection is thought to be the main cause. In older patients, luminal obstruction is more likely to be caused by fibrosis, fecaliths, or neoplasia (carcinoid, adenocarcinoma, or mucocele). In endemic areas, parasites can cause obstruction in any age group. (See "Cancer of the appendix and pseudomyxoma peritonei".)

Once obstructed, the lumen becomes filled with mucus and distends, increasing luminal and intramural pressure. This results in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. As lymphatic and vascular compromise progress, the wall of the appendix becomes ischemic and then necrotic.

Bacterial overgrowth occurs within the diseased appendix. Aerobic organisms predominate early in the course, while mixed infection is more common in late appendicitis. Common organisms involved in gangrenous and perforated appendicitis include Escherichia coli, Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species . Intraluminal bacteria subsequently invade the appendiceal wall and further propagate a neutrophilic exudate. The influx of neutrophils causes a fibropurulent reaction on the serosal surface, irritating the surrounding parietal peritoneum . This results in stimulation of somatic nerves, causing pain at the site of peritoneal irritation .

A model that separates the pathogenesis of nonperforating from perforating appendicitis has been proposed . It is thought that the type of luminal obstruction may be a predictor of appendicitis leading to perforation. Further reinforcement of this theory came from research into the types of fecaliths and calculi that can be found in the appendix. Fecaliths were six times more common than true calculi, but calculi were more often associated with perforated appendicitis or periappendiceal abscess (45 per cent) than were fecaliths (19 per cent). This is presumably due to the rigidity of true calculi as compared to the softer, more crushable fecaliths .

Once significant inflammation and necrosis occur, the appendix perforates, leading to localized abscess formation or diffuse peritonitis. During the first 24 hours after symptoms develop, approximately 90 percent of patients have inflammation and perhaps necrosis of the appendix, but not perforation.

The time course to perforation is variable. One study showed that 20 percent of patients developed perforation less than 24 hours after the onset of symptoms . Sixty-five percent of patients in whom the appendix perforated had symptoms for longer than 48 hours.

A perforated appendix must be considered in a patient whose temperature exceeds 103.0ºF (39.4ºCelsius). The same considerations apply for an elevated white blood cell count. Many patients will have a mild leukocytosis of up to 15 X 10(3)/mm(3). Perforation is more likely to have occurred in patients with a higher leukocyte count.

CLINICAL MANIFESTATIONS — Abdominal pain is the most common clinical symptom of appendicitis, and is found in nearly all confirmed cases . The clinical presentation of acute appendicitis is described as a constellation of "classic" signs and symptoms:

 • Right lower quadrant (right iliac fossa) abdominal pain

 • Anorexia

 • Nausea and vomiting

In the "classic" presentation, the patient describes the onset of abdominal pain as the first symptom. The pain is periumbilical in nature with subsequent migration to the right lower quadrant as the inflammation progresses . Nausea and vomiting, if they occur, usually follow the onset of pain. Fever and leukocytosis follow later in the course of illness. Low grade fever up to 101.0ºF (38.3ºC) may be present.

Nevertheless, in many patients, initial features are atypical or nonspecific, and can include:

 • Indigestion

 • Flatulence

 • Bowel irregularity

 • Diarrhea

 • Generalized malaise

Because the early signs and symptoms of appendicitis are often subtle, patients and clinicians may downplay their importance. Although considered a classic symptom, migratory pain that begins in the periumbilical region and then moves to the right lower quadrant occurs only in 50 to 60 percent of patients with appendicitis .

The symptoms of appendicitis can vary depending upon the location of the appendix. An inflamed anterior appendix produces marked symptoms in the right lower quadrant, while a retrocecal appendix may not cause the same degree of local signs of peritonitis because the inflammation is masked by the overlying bowel.

No single feature or combination of features is a highly accurate predictor of acute appendicitis, although prediction rules based upon combinations of features may have some clinical utility .

DIFFERENTIAL DIAGNOSIS — A variety of inflammatory conditions in the right lower quadrant can mimic appendicitis.

Cecal diverticulitis — Cecal diverticulitis usually occurs in young adults and presents with signs and symptoms that are virtually identical to those of appendicitis. 

Meckel's diverticulitis — Meckel's diverticulitis presents in a fashion similar to appendicitis. A Meckel's diverticulum is a congenital remnant of the omphalomesenteric duct. It contains all layers of the intestine and may have ectopic tissue present from either the pancreas or stomach. It is located on the small intestine two feet from the ileocecal valve, and is about two inches in length .

Meckel's diverticulitis should be included in the differential diagnosis as the small bowel may migrate into the right lower quadrant and mimic the symptoms of appendicitis. Other complications associated with a Meckel's diverticulum include bleeding if it contains ectopic gastric mucosa, and an obstruction due to the diverticulum serving as a leading edge for an intussusception or an internal hernia. If an inflamed appendix is not found on abdominal exploration for acute appendicitis, the surgeon should search for an inflamed Meckel's diverticulum. 

Acute ileitis — Acute ileitis due most commonly to an acute self-limited bacterial infection (Yersinia, Campylobacter, Salmonella, and others), should be considered when diarrhea is a prominent symptom. 

Crohn's disease — Crohn's disease can present with symptoms similar to appendicitis. Fatigue, prolonged diarrhea with abdominal pain, weight loss, and fever, with or without gross bleeding are the hallmarks of Crohn's disease. Crohn's disease should be suspected in patients who have persistent pain after surgery, especially if the appendix is histologically normal.

Gynecologic conditions — A number of gynecologic conditions, most notably ectopic pregnancy and pelvic inflammatory disease (acute salpingitis), should be considered in the differential diagnosis. 

PHYSICAL EXAMINATION — The patient should undergo a careful physical examination, including a rectal examination. Women should undergo a pelvic examination. 

The physical examination may be unrevealing in the very early stages of appendicitis since the visceral organs are not innervated with somatic pain fibers. However, as the inflammation progresses, involvement of the overlying parietal peritoneum causes localized tenderness in the right lower quadrant. This may be detected with abdominal examination, or during rectal and pelvic examination. 

Patients with a retrocecal appendix are an exception since the appendix does not come into contact with the anterior parietal peritoneum. In such patients, localized tenderness may be less impressive. These patients often complain of a dull ache instead of the localized tenderness that is seen with an inflamed appendix in the anterior iliac fossa. Rectal or pelvic examination in such patients is more likely to elicit symptoms than abdominal examination.

The location of the pain may also be atypical in patients who have a pelvic appendix, which can cause tenderness below McBurney's point. Such patients often complain of urinary frequency and dysuria or rectal symptoms, such as tenesmus and diarrhea.

Several findings on physical examination have been described to facilitate diagnosis:

 • McBurney's point tenderness is described as maximal tenderness at 1.5 to 2 inches from the anterior superior iliac spine (ASIS) on a straight line from the ASIS to the umbilicus. (Sensitivity 50 to 94 percent; specificity 75 to 86 percent ).

 • Rovsing's sign refers to pain in the right lower quadrant with palpation of the left lower quadrant. This sign is also called indirect tenderness and is indicative of right-sided local peritoneal irritation . (Sensitivity 22 to 68 percent; specificity 58 to 96 percent ).

 • The psoas sign is indicative of a retrocecal appendix. This is manifested by right lower quadrant pain with right hip flexion. The inflamed appendix may lie against the right psoas muscle, causing the patient to shorten the muscle by drawing up the right knee. Passive extension of the iliopsoas muscle with hip extension causes right lower quadrant pain. (Sensitivity 13 to 42 percent; specificity 79 to 97 percent ).

 • The obturator sign is indicative of a pelvic appendix. This test is based on the principle that the inflamed appendix may lie again the right obturator internus muscle. When the clinician flexes the patient's right hip and knee followed by internal rotation of the right hip, this elicits right lower quadrant pain. (Sensitivity 8 percent; specificity 94 percent ).

LABORATORY STUDIES — Laboratory tests serve a supportive role in the diagnosis of appendicitis as the diagnosis is made primarily on clinical findings. No single laboratory test or combination of tests is an absolute marker for appendicitis . Howwever, laboratory tests are useful and patients with an acute abdomen should have a complete blood count (CBC) with a differential to identify a leukocytosis. Approximately 80 percent of patients with appendicitis have a preoperative leukocytosis (white cells >10,000 cells/uL) and a left shift in the differential . It is important to remember that a leukocytosis can be present in other acute etiologies of abdominal pain. However, acute appendicitis is unlikely when the WBC is normal . In addition, a pregnancy test should be performed for all women of childbearing age.

Interestingly, mild elevations in serum bilirubin (total bilirubin >1.0 mg/dL) have been noted to be a marker for appendiceal perforation with a sensitivity of 70 percent and a specificity of 86 percent. This compares favorably with a sensitivity and specificity of an elevated WBC of 80 percent and 55 percent respectively.

CLINICAL ASSESSMENT — The constellation of findings from history, physical examination, and laboratory studies can often lead an experienced examiner to the correct diagnosis of appendicitis without further imaging . Several studies have found the diagnostic accuracy of clinical evaluation alone to be 75 to 90 percent . The diagnostic accuracy of the clinical examination may depend on the experience of the examining clinician .

Patients in whom appendicitis is considered to be extremely likely after assessment by an experienced clinician should proceed to appendectomy without further radiologic testing.

Diagnostic scoring systems — Several scoring systems have been proposed to standardize the correlation of clinical and laboratory variables. The Alvarado score is the most widely used diagnostic aid for the diagnosis of appendicitis and has been modified slightly since it was introduced.

The modified Alvarado scale assigns a score to each of the following diagnostic criteria:

 • Migratory right iliac fossa pain (1 point)

 • Anorexia (1 point)

 • Nausea/vomiting (1 point)

 • Tenderness in the right iliac fossa (2 points)

 • Rebound tenderness in the right iliac fossa (1 point)

 • Fever >37.5 degrees C (1 point)

 • Leukocytosis (2 points)

The points totals are used to guide management:

 • A patient with a score of 0 to 3 could be considered to have a low risk of appendicitis and would be discharged with advice to return if there was no improvement in symptoms, subject to social circumstances.

 • A patient with a score of 4 to 6 would be admitted for observation and re-examination. If the score remains the same after 12 hours, operative intervention is recommended.

 • A male patient with a score of 7 to 9 would proceed to appendectomy.

 • A female patient who is not pregnant would undergo diagnostic laparoscopy, then appendectomy if indicated by the intraoperative findings. The surgical management of appendicitis in pregnancy is discussed separately. 

In validation studies, the Alvarado score had a sensitivity of 95 percent for appendicitis with a score greater than 7 and overall accuracy of 83 percent . However, it is more accurate in men and children than in women .

Accuracy of the score appears to be lower in women . Some have advocated diagnostic laparoscopy to minimize the high false-negative rate in women . Others have suggested using CT scans to help with the diagnosis of patients with equivocal clinical presentation and a score of 4 to 6.

Several other scoring systems have been described as well . A systematic review of several published scoring systems showed a diagnostic sensitivity of 53 to 99 percent and specificity of 30 to 99 percent . As a general rule, the addition of these decision aids to clinical judgment has the potential to improve specificity and lead to lower false-positive rates in diagnosis of acute appendicitis, but decision aids cannot definitively determine or exclude the possibility of appendicitis .

RADIOGRAPHIC STUDIES — Over the last few decades, there has been increasing use of imaging modalities such as ultrasonography (US) and computed tomography (CT) in the diagnosis of acute appendicitis. Although the increased use of imaging has decreased the rate of negative appendectomies , many surgeons will proceed with surgical exploration, in the absence of imaging, if there is a strong clinical concern for appendicitis.

The acceptable number of negative appendectomies varies depending upon the age and sex of the patient. For example, in young healthy males with right lower quadrant pain, the negative appendectomy rate (NAR) should be less than 10 percent, while a rate that approaches 20 percent is reasonable in young women in whom other pelvic processes can make accurate diagnosis more difficult . A low NAR has been achieved in some centers that use close in-hospital observation .

Although diagnostic imaging is unnecessary when the diagnosis of appendicitis is certain, imaging should be performed when the diagnosis of appendicitis is suspected but unclear. Diagnostic imaging is especially useful in several subpopulations, including children, elder adults, or women of childbearing age. Similarly, patients with comorbidities such as diabetes, obesity, and immunocompromise may have a higher occurrence of atypical presentation of appendicitis. These populations are more likely to present with unclear symptoms such as vague abdominal pain.

Women of childbearing age, as well as elder adults, have a higher rate of negative appendectomy. Several studies have demonstrated that women were more than twice as likely as men to undergo a negative appendectomy and therefore benefit from standardized imaging in the evaluation of suspected appendicitis . A study of 1425 consecutive patients undergoing appendectomy over a seven-year period at a single institution found that preoperative CT scanning was particularly useful in women and contributed to a significant reduction in NAR (from 21 to 8 percent) .

Imaging is also useful for elder adults and patients with significant comorbidities, in whom the clinical findings may be atypical for appendicitis.

Computed tomography (CT) — Many studies have evaluated the diagnostic accuracy of CT scan for appendicitis in comparison to clinical examination. Patients with suspected appendicitis can often be categorized into those with clinical findings that are highly predictive of the presence or absence of appendicitis and those with an equivocal clinical picture. Some studies comparing evaluation by surgical attendings with findings of CT scan have found statistically similar diagnostic accuracy in the assessment of patients presenting with an equivocal examination . Other studies have found that CT findings influence the treatment plan; in one such report, the CT scan changed the treatment plan for 58 percent of patients . Differences in studies may in part be due to the experience of the clinical assessor and the populations being studied.

Several CT protocols for imaging the appendix have been described, three protocols are mainly used. These include:

 • Standard abdominal-pelvic CT with IV and oral contrast

 • Focused appendiceal CT with rectal contrast

 • Non-contrast CT

In most cases, if there is enough diagnostic concern and uncertainty to warrant a CT scan for appendicitis, a full abdominal-pelvic CT with IV and oral contrast should be performed or a decision should be made to proceed to the operating room for abdominal exploration.

Standard CT with contrast — A commonly used protocol involves a standard abdominal and pelvic CT scan (16-MDCT or higher) with intravenous and oral contrast. 

A number of findings suggest acute appendicitis on standard abdominal CT scanning :

 • Enlarged appendiceal diameter >6 mm with an occluded lumen

 • Appendiceal wall thickening (>2 mm)

 • Periappendiceal fat stranding

 • Appendiceal wall enhancement

 • Appendicolith 

The sensitivity and specificity of CT with IV and oral contrast for acute appendicitis is in the range of 91 to 98 and 75 to 93 percent, respectively . Air in the appendix or a contrast filled lumen in a normal appearing appendix virtually excludes the diagnosis. However, a nonvisualized appendix does not rule out appendicitis. This is particularly important to remember in patients who have had symptoms for a short duration, since only minimal inflammatory changes may be present in the right lower quadrant.

An advantage of a complete abdominal CT scan is that it permits visualization of the entire abdomen. An alternative diagnosis is found in up to 15 percent of patients . Furthermore, a CT scan can assist in the treatment plan for patients with a palpable abdominal mass, such as those in whom an appendiceal phlegmon or abscess may have developed. These features are more likely in patients who present after having prolonged symptoms (four to five days).

A drawback of the standard CT protocol is that it takes up to two hours to administer oral contrast. In addition a CT scan involves radiation exposure and intravenous contrast, with the potential for contrast-induced renal nephropathy. Cost and availability are also considerations, particularly in resource-poor settings.

Appendiceal CT — A focused appendiceal CT scan can be performed with rectal contrast alone and thin cuts through the right iliac fossa. Because full oral contrast is not given, the scan can be performed within 15 minutes. Rectal contrast provides good visualization of the pericecal region without the need to wait for oral contrast to reach the right lower quadrant.

In a report using a limited appendiceal CT scan with rectal contrast, the sensitivity of the most common findings for acute appendicitis were as follows :



 • Right lower abdominal quadrant fat stranding (100 percent sensitivity)

 • Focal cecal thickening (69 percent specificity)

 • Adenopathy (63 percent sensitivity)

One study reported that a focal appendiceal CT had 98 percent accuracy and sensitivity with rectal contrast along a limited area (15 cm) of the pelvis centered 3 cm superior to the cecal tip.

The relevance of focal appendiceal imaging is questionable outside of large medical centers, as this technique requires personnel to administer rectal contrast and a radiologist on site for the verification of positioning. In addition, an appendiceal CT scan only looks at the appendix, and the images may be unrevealing in the presence of other abdominal pathology. As a result, evaluation should continue in patients with a negative study.

Unenhanced CT — The administration of contrast for imaging adds time, expense, and risk of an allergic reaction to the contrast agent. A number of studies have suggested that adequate imaging can be obtained without contrast. In various reports, unenhanced CT had a sensitivity of 88 to 96 percent, specificity of 91 to 98 percent, and diagnostic accuracy of 94 to 97 percent for appendicitis, with the added advantage of total exam time of 5 to 15 minutes.

Test characteristics may depend at least in part upon the patient's body habitus . Some radiologists maintain that if the BMI exceeds 25 that the CT is less accurate and therefore oral contrast is necessary.

An important limitation of unenhanced CT is the limited ability to diagnose other abdominal pathology, potentially diminishing the role of the examination in patients in whom there is diagnostic uncertainty (ie, those in whom imaging may be most important).

Unenhanced CT may be of some value in patients who have renal failure or clinical instability. However, for most patients where there is sufficient diagnostic uncertainty to warrant a CT scan for appendicitis, a full abdominal-pelvic CT with IV and oral contrast should be performed or a decision should be made to proceed to the operating room for abdominal exploration.

Ultrasonography — Ultrasound (US) is generally considered to be reliable for ruling-in acute appendicitis, but cannot be trusted to rule it out. It has little added value when the clinical presentation is clear.

At least eight sonographic internal inflammatory changes of the appendix have been described [11,43,88]. The most accurate ultrasound finding for acute appendicitis is an appendiceal diameter of >6 mm with a sensitivity, specificity, negative predictive value and positive predictive value of 98 percent. In various reports, the sensitivity and specificity by US in the diagnosis of appendicitis ranged from 35 to 98 percent and 71 to 98 percent, respectively .

Advantages compared with CT include the ability to obtain results quickly, and lack of radiation exposure or need for contrast agents. An added benefit is that it can also be useful for defining pelvic pathology in women. Endovaginal ultrasound is particularly sensitive for evaluating the female reproductive tract. The roles of ultrasonography in evaluation of appendicitis during pregnancy and in children are described separately. 

The disadvantages of ultrasonography are that it is not as accurate as CT for diagnosis of appendicitis and is less likely to reveal alternative diagnoses. Furthermore, accuracy is operator dependent and it may be difficult to image patients with a large body habitus or those who have a large amount of overlying bowel gas. As a general rule, the main role of ultrasonography is to help confirm the diagnosis of suspected appendicitis, particularly in women.

Plain radiographs — Plain radiographs are usually not helpful for establishing the diagnosis of appendicitis. However, the following radiographic findings have been associated with acute appendicitis:

 • Right lower quadrant appendicolith

 • Localized right lower quadrant ileus

 • Loss of the psoas shadow

 • Free air (occasionally)

 • Deformity of cecal outline

 • Right lower quadrant soft tissue density

Imaging costs — The increase in the use of CT scanning for the diagnosis of appendicitis has been largely justified by the assumption that it decreases the rates of perforated appendicitis as well as nontherapeutic appendectomies . In two studies that performed cost analysis, one showed that the cost of nontherapeutic appendectomy was 16 times more expensive than a focused appendiceal CT scan, while another reported that appendectomy was 22 times more expensive than non-enhanced CT scanning, implying cost savings if a reduction in nontherapeutic appendectomy rates could be achieved .

Several studies have failed to demonstrate a significant reduction in the overall institutional rates for nontherapeutic appendectomies despite the increased use of CT scan over time. Results of studies that included analysis of perforated appendicitis are mixed. One study showed an observed rate of appendiceal perforation of 9 percent in patients who underwent routine CT imaging compared to 25 percent in patients in whom CT scanning was not used . Other studies have demonstrated a fairly constant rate of perforated appendix over time despite the increased use of CT scan.

Cost analysis for studies such as these is complicated by the value of CT scanning in patients in whom therapeutic appendectomy was performed; as a result, the cost savings depends upon an absolute rate reduction for nontherapeutic appendectomies . Additionally, cost calculations depend upon local institutional variables and surgeon variables; selected institutional observations may not be applicable to all practices.

SUMMARY AND RECOMMENDATIONS

 • Acute appendicitis is one of the most common causes of an acute abdomen. The goal of therapy is early diagnosis and prompt operative intervention.

 • The position of the appendix can vary significantly between individuals. The appendix can be found in a retrocecal or pelvic location, as well as medial, lateral, anterior or posterior to the cecum. Anatomic variability can complicate the diagnosis as clinical presentation will reflect the anatomic position of the appendix.

 • Appendiceal obstruction plays a role in the pathogenesis of appendicitis, but it is not required for the development of appendicitis.

 • The "classic" symptoms of appendicitis include right lower quadrant abdominal pain, anorexia, fever, nausea and vomiting. The abdominal pain is initially periumbilical in nature with subsequent migration to the right lower quadrant as the inflammation progresses.

 • Not all patients will appendicitis will have the "classic" symptoms. Many patients with appendicitis present with atypical or nonspecific symptoms, such as indigestion, flatulence, bowel irregularity, and generalized malaise. Not all patients will have migratory pain and symptoms can vary depending upon the location of the appendix, especially when the appendix is retrocecal or pelvic. (See 'Clinical manifestations' above.)

 • The constellation of findings from history, physical examination, and laboratory studies will usually lead an experienced examiner to the correct diagnosis of appendicitis without further imaging. Diagnostic scoring systems can be helpful in the diagnosis of acute appendicitis but cannot definitively rule out the possibility of appendicitis.

 • Patients in whom appendicitis is considered to be extremely likely after assessment by an experienced clinician should proceed to appendectomy without further radiologic testing. A diagnostic laparoscopy should be considered for women of child-bearing age as this can help minimize the negative appendectomy rate.

 • Diagnostic imaging should be performed when the diagnosis of appendicitis is suspected but unclear. We suggest a standard abdominal CT scan with intravenous and oral or rectal contrast. 

 • A variety of inflammatory conditions in the right lower quadrant can mimic appendicitis and should be considered in differential diagnosis.
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